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Cells
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Glycative Stress and Anti-glycative Mechanisms in Aging and Age-Related Diseases
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Glycative Stress and Anti-glycative Mechanisms in Aging and Age-Related Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Aging".

Deadline for manuscript submissions: closed (20 December 2023) | Viewed by 7414

Special Issue Editors

Dr. Eloy Bejarano

E-Mail Website
Guest Editor
School of Health Sciences, Universidad CEU Cardenal Herrera, 46115 Alfara del Patriarca, Spain
Interests: proteostasis; aging; nutrition; autophagy; glycation
Prof. Dr. Allen Taylor

E-Mail Website
Guest Editor
School of Nutrition Science and Policy, Tufts University Friedman, 150 Harrison Avenue, Boston, MA 02111, USA
Interests: autophagy; age-related eye diseases

Special Issue Information

Dear Colleagues,

Glycation is a non-enzymatic process by which sugars or sugar metabolites are covalently bound to proteins, lipids, and DNA. Glycated biomolecules are generated in hyperglycemic states, which occur in diabetes mellitus and upon the consumption of high-sugar diets in non-diabetics, particularly in older individuals. In order to combat glycative stress, there are different defense mechanisms against the accumulation of advanced glycation end products (AGEs). However, the age-related decline in the function of these activities results in glycative modification and damage upon aging and age-related diseases. Such damage may be etiologic for aging and age-related diseases. Exploring the role of anti-AGEs mechanisms in different tissues/organs in the context of aging will help to elucidate the cellular basis of glycative stress in age-related diseases and inform the development of future therapeutic tools.

This Special Issue will highlight glycation-related topics, including:

  • Pathological impact of glycative stress in human diseases and diabetes complications
  • In vivo and in vitro models for studying the pathological impact of glycative stress.
  • Enzymatic systems limiting the glycation process (glyoxalase system, Park7/DJ-1, etc.) and the proteolytic pathways involved in AGE clearance (autophagy, UPS).
  • The health benefits of the use of nutrition, phytocompounds, and pharmacological drugs to combat glycative stress.
  • Novel analytical methods for evaluating glycative stress.
  • Epidemiological studies providing information about glycation-related complications.

Dr. Eloy Bejarano
Prof. Dr. Allen Taylor
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • diabetes
  • aging
  • nutrition
  • diet
  • advanced glycation end products
  • glyoxalase system
  • anti-glycating agents

Published Papers (4 papers)

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Research

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13 pages, 2218 KiB  
Communication
Oleic Acid Status Positively Correlates with the Soluble Receptor for Advanced Glycation End-Products (sRAGE) in Healthy Adults Who Are Homozygous for G Allele of RAGE G82S Polymorphism
by Permal Deo, Varinderpal S. Dhillon, Philip Thomas and Michael Fenech
Cells 2023, 12(12), 1662; https://doi.org/10.3390/cells12121662 - 19 Jun 2023
Cited by 1 | Viewed by 952
Abstract
Background: The soluble form of receptor for advanced glycation end products (sRAGE) have been implicated in the prevention of numerous pathologic states, and highlights as an attractive therapeutic target. Because diets rich in monounsaturated fatty acids (MUFA) reduce postprandial oxidative stress and inflammation [...] Read more.
Background: The soluble form of receptor for advanced glycation end products (sRAGE) have been implicated in the prevention of numerous pathologic states, and highlights as an attractive therapeutic target. Because diets rich in monounsaturated fatty acids (MUFA) reduce postprandial oxidative stress and inflammation that is related to better health during aging, we investigated the association between red blood cell (RBC) fatty acids with circulatory AGE biomarkers and further stratified this correlation based on GG and GA + AA genotype. Methods: A total of 172 healthy participants (median age = 53.74 ± 0.61 years) were recruited for the study. RBC fatty acid was analysed using gas chromatography and sRAGE was measured using a commercial ELISA kit. Results: The result showed a non-significant correlation between total MUFA with sRAGE however oleic acid (C18:1) exhibited a positive correlation (r = 0.178, p = 0.01) that remained statistically significant (β = 0.178, p = 0.02) after a stepwise multivariate regression analysis after adjusting for age, BMI and gender. In a univariate analysis, a positive significant correlation between C18:1 and sRAGE in GG genotype (r = 0.169, p = 0.02) and a non-significant correlation with GA + AA genotype (r = 0.192, p = 0.21) was evident. When C18:1 was stratified, a significant difference was observed for oleic acid and G82S polymorphism: low C18:1/GA + AA versus high C18:1/GG (p = 0.015) and high C18:1/GA + AA versus high C18:1/GG (p = 0.02). Conclusion: Our study suggests that increased levels of C18:1 may be a potential therapeutic approach in increasing sRAGE in those with GG genotype and play a role in modulating AGE metabolism. Full article
(This article belongs to the Special Issue Glycative Stress and Anti-glycative Mechanisms in Aging and Age-Related Diseases)
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12 pages, 575 KiB  
Article
Association of Autofluorescent Advanced Glycation End Products (AGEs) with Frailty Components in Chronic Kidney Disease (CKD): Data from a Single-Center Cohort Study
by Paolo Molinari, Lara Caldiroli, Elena Dozio, Roberta Rigolini, Paola Giubbilini, Francesca Maria Ida Carminati, Giuseppe Castellano, Massimiliano M. Corsi Romanelli and Simone Vettoretti
Cells 2023, 12(3), 438; https://doi.org/10.3390/cells12030438 - 29 Jan 2023
Cited by 1 | Viewed by 1246
Abstract
Background: Chronic kidney disease (CKD) is characterized by an overproduction and accumulation of advanced glycation end products (AGEs). Because AGEs may play a role in the development of malnutrition and sarcopenia, two essential components of frailty, we evaluated whether they may also contribute [...] Read more.
Background: Chronic kidney disease (CKD) is characterized by an overproduction and accumulation of advanced glycation end products (AGEs). Because AGEs may play a role in the development of malnutrition and sarcopenia, two essential components of frailty, we evaluated whether they may also contribute to the onset of frailty in CKD patients. Methods: We performed a cross-sectional analysis of 117 patients. AGEs were quantified using a fluorescence spectrophotometer and soluble receptor for AGE (sRAGE) isoforms by ELISA. We defined frailty according to the frailty phenotype (FP) proposed by Fried. Results: The average age of patients was 80 ± 11 years, 70% were male, and the mean eGFR was 25 + 11 mL/min/1.73m2. Frailty was diagnosed in 51 patients, and 40 patients were classified as pre-frail. AGEs and RAGE isoforms seem not to correlate with overall frailty. Instead, AGEs were associated with specific frailty domains, inversely associated with BMI (R = −0.22, p = 0.016) and directly associated with gait test time (R = 0.17, p = 0.049). AGEs were also associated with involuntary weight loss (OR 1.84 p = 0.027), independent of age and sex. Conclusions: AGEs are associated with some pivotal components of the frailty phenotype, although they are not associated with frailty overall. Full article
(This article belongs to the Special Issue Glycative Stress and Anti-glycative Mechanisms in Aging and Age-Related Diseases)
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Review

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13 pages, 317 KiB  
Review
Dietary Advanced Glycation End Products: Their Role in the Insulin Resistance of Aging
by Manuel Portero-Otin, M. Pia de la Maza and Jaime Uribarri
Cells 2023, 12(13), 1684; https://doi.org/10.3390/cells12131684 - 21 Jun 2023
Cited by 4 | Viewed by 1389
Abstract
Insulin resistance (IR) is commonly observed during aging and is at the root of many of the chronic nontransmissible diseases experienced as people grow older. Many factors may play a role in causing IR, but diet is undoubtedly an important one. Whether it [...] Read more.
Insulin resistance (IR) is commonly observed during aging and is at the root of many of the chronic nontransmissible diseases experienced as people grow older. Many factors may play a role in causing IR, but diet is undoubtedly an important one. Whether it is total caloric intake or specific components of the diet, the factors responsible remain to be confirmed. Of the many dietary influences that may play a role in aging-related decreased insulin sensitivity, advanced glycation end products (AGEs) appear particularly important. Herein, we have reviewed in detail in vitro, animal, and human evidence linking dietary AGEs contributing to the bodily burden of AGEs with the development of IR. We conclude that numerous small clinical trials assessing the effect of dietary AGE intake in combination with strong evidence in many animal studies strongly suggest that reducing dietary AGE intake is associated with improved IR in a variety of disease conditions. Reducing AGE content of common foods by simple changes in culinary techniques is a feasible, safe, and easily applicable intervention in both health and disease. Large-scale clinical trials are still needed to provide broader evidence for the deleterious role of dietary AGEs in chronic disease. Full article
(This article belongs to the Special Issue Glycative Stress and Anti-glycative Mechanisms in Aging and Age-Related Diseases)
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22 pages, 1852 KiB  
Review
Effects of Toxic AGEs (TAGE) on Human Health
by Masayoshi Takeuchi, Akiko Sakasai-Sakai, Takanobu Takata, Jun-ichi Takino and Yoshiki Koriyama
Cells 2022, 11(14), 2178; https://doi.org/10.3390/cells11142178 - 12 Jul 2022
Cited by 10 | Viewed by 2792
Abstract
The habitual and excessive consumption of sugar (i.e., sucrose and high-fructose corn syrup, HFCS) is associated with the onset and progression of lifestyle-related diseases (LSRD). Advanced glycation end-products (AGEs) have recently been the focus of research on the factors contributing to LSRD. Approaches [...] Read more.
The habitual and excessive consumption of sugar (i.e., sucrose and high-fructose corn syrup, HFCS) is associated with the onset and progression of lifestyle-related diseases (LSRD). Advanced glycation end-products (AGEs) have recently been the focus of research on the factors contributing to LSRD. Approaches that inhibit the effects of AGEs may be used to prevent and/or treat LSRD; however, since the structures of AGEs vary depending on the type of reducing sugars or carbonyl compounds to which they respond, difficulties are associated with verifying that AGEs are an etiological factor. Cytotoxic AGEs derived from glyceraldehyde, a triose intermediate in the metabolism of glucose and fructose, have been implicated in LSRD and are called toxic AGEs (TAGE). A dietary imbalance (the habitual and excessive intake of sucrose, HFCS, or dietary AGEs) promotes the generation/accumulation of TAGE in vivo. Elevated circulating levels of TAGE have been detected in non-diabetics and diabetics, indicating a strong relationship between the generation/accumulation of TAGE in vivo and the onset and progression of LSRD. We herein outline current findings on “TAGE as a new target” for human health. Full article
(This article belongs to the Special Issue Glycative Stress and Anti-glycative Mechanisms in Aging and Age-Related Diseases)
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